Parasite Immunology最新文献

Chicken coccidiosis, caused by Eimeria protozoa, affects poultry farming. Toll-like receptors (TLRs) and host defence peptides (HDPs) help host innate immune responses to eliminate invading pathogens, but their roles in Eimeria tenella infection remain poorly understood. Herein, 14-day-old chickens were treated orally with 50,000 E. tenella oocysts and the cecum was dissected at different timepoints. mRNA expression of 10 chicken TLRs (chTLRs) and five HDPs was measured by quantitative real-time PCR. chTLR7 and chTLR15 were upregulated significantly at 3 h post-infection while other chTLRs were downregulated (p < .05). chTLR1a, chTLR1b, chTLR2b and chTLR4 peaked at 36 h post-infection, chTLR3, chTLR5 and chTLR15 peaked at 72 h post-infection and chTLR21 expression was highest among chTLRs, peaking at 48 h post-infection (p < 0.05). For HDPs, cathelicidin (CATH) 1 to 3 and B1 peaked at 48 h post-infection, liver-expressed antimicrobial peptide 2 peaked at 96 h post-infection, and CATH 2 expression was highest among HDPs. CATH2 and CATH3 were markedly upregulated at 3 h post-infection (p < .05). The results provide insight into innate immune molecules during E. tenella infection in chicken, and indicate that innate immune responses may mediate resistance to chicken coccidiosis.

Inducing long-term immunity is the primary goal of vaccination. Leishmanisation using non-pathogenic to human Leishmania spp. could be considered a reliable approach to immunising subjects against Leishmania infection. Here, we evaluated the long-term immune responses (14 weeks) after immunisation with either live- or killed-Iranian Lizard Leishmania (ILL) mixed with chitin microparticles (CMPs) against L. major infection in BALB/c mice. In total, nine groups of mice were included in the study. To evaluate short-term immunity, mice were immunised with live-ILL and CMPs and 3 weeks later were challenged with L. major^EGFP . To evaluate the long-term immunity, mice were immunised with either live- or killed-ILL both mixed with CMPs, and 14 weeks after immunisation, mice were challenged with L. major^EGFP . A group of healthy mice who received no injection was also included in the study. Eight weeks after the challenge with L. major^EGFP , all subjects were sacrificed and the parasite burden (quantitative real-time PCR and in vivo imaging), cytokines levels (IFN-γ, IL-4 and IL-10), Leishmania-specific antibody concentration, and total levels of IgG1 and IgG2a were measured. In addition, nitric oxide concentration and arginase activity were evaluated. Results showed that in mice that were immunised using live-ILL+CMP, the induced protective immune response lasted at least 14 weeks; since they were challenged with L. major^EGFP at the 14^th -week post-immunisation, no open lesion was formed during the 8-week follow-up, and the footpad swelling was significantly lower than controls. They also showed a significant reduction in the parasite burden in splenocytes, compared to the control groups including the group that received killed-ILL+CMP. The observed protection was associated with a higher IFN-γ and a lower IL-10 production by splenocytes. Additionally, the results demonstrated that arginase activity was decreased in the ILL+CMP group compared to other groups. Immunisation with ILL alone reduced the parasite burden compared to non-immunised control; however, it was still significantly higher than the parasite burden in the ILL+CMP groups. In conclusion, the long-term immune response against L. major infection induced by Live-ILL+CMP was more competent than the response elicited by killed-ILL+CMP to protect mice against infection with L. major^EGFP .

Complement is the first line of the host innate immune response against bacterial and viral infections; however, its role in the development of the malaria liver stage remains undefined. We found that sporozoite infection by either a mosquito bite or intravenous injection activated systemic complement, but neither depletion of C3 nor knockout of C3 had a significant effect on malaria liver stage development. Incubation of mouse serum with trypsin-treated sporozoites, but not naive sporozoites, led to the deposition of a membrane attack complex (MAC) on the surface of sporozoites and greatly reduced the number of exo-erythrocytic forms (EEF). Further studies have shown that the recruitment of complement H factor (CFH) may be associated with the prevention of MAC deposition on the surface of naïve sporozoites. Our data strongly suggest that sporozoites can escape complement attacks and provide us with a novel strategy to prevent malaria infection.

Nonspecific hypergammaglobulinemia (HGG) occurs in symptomatic human visceral leishmaniasis (VL) caused by L. L. infantum. This study assessed this finding in experimental infection in hamsters and natural infection in dogs. The serum concentration of proteins, albumin and globulins was determined through the biuret and bromocresol green reaction, where the HGG was better expressed through the albumin/globulin (A/G) ratio. HGG was associated with a higher concentration of specific anti-glycan antibodies (BSA-G)/promastigote soluble extract (PSE) and the presence of circulating immune complexes (IC) by dissociative enzyme-linked immunoassay (ELISA). The study found monovalent IC in 37.9% (PSE) and 50% (BSA-G) of sera from infected hamsters, with increased frequency as the disease progressed. HGG was found in >60% of the samples in dogs with VL, associated with higher levels of specific immunoglobulin (Ig)A and IgM, but not IgG, determined using the PSE and BSA-G ELISA. HGG was associated with the presence of monovalent IC in 58.9% (PSE) and 63.4% (BSA-G) positive dog samples. HGG may result not only from the nonspecific activation of B cells, with greater production of specific and nonspecific antibodies, but also due to lower IgG excretion due to the presence of soluble monovalent IC. HGG correlates to the progression of VL and may be a marker for manifested disease.

Soil-transmitted helminths (STHs) parasitic infection is known as one of the most common infections around the world affecting more than a quarter of the world's population. The relationship between STH infections and micronutrient deficiencies are closely related and often coexist among the affected population. The study, therefore, aimed to summarise the available literature focusing on the effect of zinc status/deficiency or supplementation on STH infection or reinfection in children. For this purpose, we adopted a systematic approach and searched the existing literature on PubMed, Scopus, and Cochrane Library databases. A search term was entered to retrieve the available data. A total of 12 articles were included in this review after applying the inclusion/exclusion criteria. Most of the included studies reported a lower zinc status in children affected with any parasitic infection. Regarding the effect of zinc status and supplementation on parasitic infection in children, we found only a few studies (n = 4) with inconsistent result findings. This review reported that children infected with STH have lower zinc levels; however, a limited number of studies showed the effect of zinc supplements on the risk of STH warrants the need for further studies in this regard.

Mucormycosis is a fungal infection caused by moulds from the Mucorales order. Concerns have been mounting due to the alarming increase in severe morbidity and mortality associated with mucormycosis during the COVID-19 pandemic. This condition, known as COVID-19-associated mucormycosis (CAM), has been linked to various environmental, host-related, and medical factors on a global scale. We have categorized the most significant potential risk factors for developing mucormycosis in individuals with a previous history of coronavirus infection into 10 major categories. These categories include acute hyperglycemia, the impact of cytokine release, immune response deficiencies in COVID-19 patients, microvasculopathy and dysfunction of endothelial cells, imbalances in iron metabolism, metabolic acidosis, organ damage resulting from COVID-19, underlying health conditions (such as diabetes), environmental factors, and medical treatments that can be iatrogenic in nature (such as inappropriate glucocorticoid use). Many of these factors can lead to potentially life-threatening infections that can complicate the treatment of COVID-19. Physicians should be vigilant about these factors because early detection of mucormycosis is crucial for effective management of this condition.

A role of IL-10 is down-regulating T-cell responses to schistosome antigens. Since SmATPDases can be correlated to modulation of the immune response, we evaluated the expression of enzymes in S. mansoni eggs. Faecal samples were collected from 40 infected individuals to detect coding regions of the SmATPDases. The cytokines were measured in supernatants of PBMC. The analysis was performed by the global median determination and set up high producers (HP) of cytokines. Six individuals expressed SmATPDase1, six expressed SmATPDase2 and six expressed both enzymes. The group who expressed only SmATPDase1 showed a high frequency of IFN-γ, TNF IL-4 HP; individuals who expressed only SmATPDase2 showed a high frequency of IFN-γ, IL-6 and IL-4 HP; and individuals who expressed both enzymes showed a high frequency of IL-10 HP. The comparison of the IFN-γ/IL-10 ratio presented higher indices in the group who had SmATPDase 2 expression than those who had the expression of both enzymes. The positive correlation between infection intensity and IL-10 levels remained only in the positive SmATPDase group. The IL-10 is the only cytokine induced by the expression of both enzymes. Our data suggest that the expression of both enzymes seems to be a factor that modulates the host immune response by inducing high IL-10 production.

This study investigated a 'de Novo' medicinal herb, Ferula asafetida (FA), against toxoplasma encephalitis either alone or combined with spiramycin (SP). Female Swiss-Webster mice (n = 72) were divided into three batches. Batch-I received no DMS to serve as an immunocompetent control, batch-II was immune-suppressed with the DMS (0.25 mg/g/day) for 14 days pre-infection, whilst batch-III was immune-suppressed with the DMS on the same day of infection. All experimental mice were inoculated with Toxoplasma gondii ME49 cysts (n = 75). Each batch was split into four subgroups: Mono-SP, mono-FA, combined drug (SP + FA), or neither. Therapies were administered on day zero of infection in batches (I and II) and 35 days post-infection in batch (III). Treatments lasted for 14 days, and mice were sacrificed 60 days post-infection. Histopathological changes, cysts load, and CD4 and CD8 T-cells were counted in brain tissues. The cyst-load count in mice receiving SP + FA was significantly (p < .0001) the least compared to the mono treatments in all protocols. Interestingly, the combined therapy demolished the T-cell subsets to zero in immunocompetent and immunocompromised infected mice. In conclusion, F. asafetida might be a powerfully natural, safe vehicle of SP in the digestive system and/or across the brain-blood barrier to control toxoplasmosis even through immunodeficient conditions.